Enterovirus 71 Infection of Human Immune Cells Induces the Production of Proinflammatory Cytokines

Lien-Cheng Chen; Trai-Ming Yeh

Enterovirus 71 Infection of Human Immune Cells Induces the Production of Proinflammatory Cytokines

貢獻的翻譯標題: 腸病毒71型感染人類免疫細胞引起發炎細胞激素的產生

Lien-Cheng Chen, Trai-Ming Yeh

醫學檢驗生物技術學系

研究成果: Article › 同行評審

摘要

發炎細胞激素風暴被認爲和腸病毒71型感染引起死亡的致病機轉有關，但對於腸病毒71型感染引起發炎細胞激素的機制仍不清楚。因爲大多數的發炎細胞激素是由免疫細胞產生，因此在本篇我們測試腸病毒71型是否可以感染人類免疫細胞並產生發炎細胞激素，我們使用RT-PCR及免疫螢光法證實腸病毒71型可以感染人類T細胞株(Jurkat)、巨嗜細胞株(THP-1)和新鮮分離的周邊血液單核性細胞，並引起發炎細胞激素腫瘤壞死因子及巨嗜細胞移動抑制因子的產生。經紫外線照射後不活化的腸病毒71型及加入actinomycin D皆會抑制這些發炎細胞激素的產生，RT-PCR也進一步證實這些發炎細胞激素的產生需要新合成的mRNA；從上述結果我們認爲腸病毒71型感染人類免疫細胞並產生發炎細胞激素可能和腸病毒71型感染引起的發炎細胞激素風暴有關。

貢獻的翻譯標題	腸病毒71型感染人類免疫細胞引起發炎細胞激素的產生
原文	English
頁（從 - 到）	82-90
期刊	Journal of Biomedical & Laboratory Sciences ＝生物醫學暨檢驗科學雜誌
卷	21
發行號	3
出版狀態	Published - 2009 9月 1

引用此

@article{44141ae1099d44e48ba58f22592a1dbe,

title = "Enterovirus 71 Infection of Human Immune Cells Induces the Production of Proinflammatory Cytokines",

abstract = "A proinflammatory cytokine storm has been proposed to explain the pathogenesis of enterovirus 71 (EV71)-induced fatalities; however, the mechanism to induce these cytokines during EV71 infection remains unclear. Since most of the proinflammatory cytokines are produced by immune cells, we tested whether EV71 infects human immune cells and induces cytokine production. EV71 infection of a human T cell line (Jurkat), macrophage cell line (THP-1), and freshly isolated human peripheral blood mononuclear cells was demonstrated using RT-PCR and immunofluorescence assays in vitro. In addition, live but not UV-inactivated EV71 increased the secretion of two proinflammatory cytokines, tumor necrosis factor-α (TNF-α) and macrophage migration inhibitory factor (MIF) by immune cells, which was inhibited in the presence of actinomycin D. RT-PCR further confirmed that EV71 infection of immune cells triggered the de novo synthesis of MIF mRNA. Therefore, our results suggest that the production of TNF-α and MIF induced by EV71 infection of immune cells may contribute to the proinflammatory cytokine storm during EV71 infection.",

author = "Lien-Cheng Chen and Trai-Ming Yeh",

year = "2009",

month = sep,

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language = "English",

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journal = "Journal of Biomedical & Laboratory Sciences ＝生物醫學暨檢驗科學雜誌",

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AU - Chen, Lien-Cheng

AU - Yeh, Trai-Ming

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N2 - A proinflammatory cytokine storm has been proposed to explain the pathogenesis of enterovirus 71 (EV71)-induced fatalities; however, the mechanism to induce these cytokines during EV71 infection remains unclear. Since most of the proinflammatory cytokines are produced by immune cells, we tested whether EV71 infects human immune cells and induces cytokine production. EV71 infection of a human T cell line (Jurkat), macrophage cell line (THP-1), and freshly isolated human peripheral blood mononuclear cells was demonstrated using RT-PCR and immunofluorescence assays in vitro. In addition, live but not UV-inactivated EV71 increased the secretion of two proinflammatory cytokines, tumor necrosis factor-α (TNF-α) and macrophage migration inhibitory factor (MIF) by immune cells, which was inhibited in the presence of actinomycin D. RT-PCR further confirmed that EV71 infection of immune cells triggered the de novo synthesis of MIF mRNA. Therefore, our results suggest that the production of TNF-α and MIF induced by EV71 infection of immune cells may contribute to the proinflammatory cytokine storm during EV71 infection.

AB - A proinflammatory cytokine storm has been proposed to explain the pathogenesis of enterovirus 71 (EV71)-induced fatalities; however, the mechanism to induce these cytokines during EV71 infection remains unclear. Since most of the proinflammatory cytokines are produced by immune cells, we tested whether EV71 infects human immune cells and induces cytokine production. EV71 infection of a human T cell line (Jurkat), macrophage cell line (THP-1), and freshly isolated human peripheral blood mononuclear cells was demonstrated using RT-PCR and immunofluorescence assays in vitro. In addition, live but not UV-inactivated EV71 increased the secretion of two proinflammatory cytokines, tumor necrosis factor-α (TNF-α) and macrophage migration inhibitory factor (MIF) by immune cells, which was inhibited in the presence of actinomycin D. RT-PCR further confirmed that EV71 infection of immune cells triggered the de novo synthesis of MIF mRNA. Therefore, our results suggest that the production of TNF-α and MIF induced by EV71 infection of immune cells may contribute to the proinflammatory cytokine storm during EV71 infection.

M3 - Article

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JO - Journal of Biomedical & Laboratory Sciences ＝生物醫學暨檢驗科學雜誌

JF - Journal of Biomedical & Laboratory Sciences ＝生物醫學暨檢驗科學雜誌

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Enterovirus 71 Infection of Human Immune Cells Induces the Production of Proinflammatory Cytokines

摘要

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